Accessibility navigation


Hypoxia suppresses astrocyte glutamate transport independently of amyloid formation

Boycott, H. E., Dallas, M., Boyle, J. P., Pearson, H. A. and Peers, C. (2007) Hypoxia suppresses astrocyte glutamate transport independently of amyloid formation. Biochemical and Biophysical Research Communications, 364 (1). pp. 100-104. ISSN 0006-291X

Full text not archived in this repository.

It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing.

To link to this item DOI: 10.1016/j.bbrc.2007.09.102

Abstract/Summary

Sustained hypoxia alters the expression of numerous proteins and predisposes individuals to Alzheimer's disease (AD). We have previously shown that hypoxia in vitro alters Ca2+ homeostasis in astrocytes and promotes increased production of amyloid beta peptides (Abeta) of AD. Indeed, alteration of Ca2+ homeostasis requires amyloid formation. Here, we show that electrogenic glutamate uptake by astrocytes is suppressed by hypoxia (1% O2, 24h) in a manner that is independent of amyloid beta peptide formation. Thus, hypoxic suppression of glutamate uptake and expression levels of glutamate transporter proteins EAAT1 and EAAT2 were not mimicked by exogenous application of amyloid beta peptide, or by prevention of endogenous amyloid peptide formation (using inhibitors of either beta or gamma secretase). Thus, dysfunction in glutamate homeostasis in hypoxic conditions is independent of Abeta production, but will likely contribute to neuronal damage and death associated with AD following hypoxic events.

Item Type:Article
Refereed:Yes
Divisions:Faculty of Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy
No Reading authors. Back catalogue items
ID Code:30357
Uncontrolled Keywords:Glia; Glutamate transport; Hypoxia; Alzheimer’s; Amyloid
Publisher:Elsevier

University Staff: Request a correction | Centaur Editors: Update this record

Page navigation